DNQX disodium salt
Chemical Name: 6,7-Dinitroquinoxaline-2,3-dione disodium salt
Biological ActivityDNQX disodium salt is a water-soluble form of DNQX (Cat. No. 0189). Selective non-NMDA receptor antagonist.
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For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Quinoxalinediones: potent competitive non-NMDA glutamate receptor antagonists.
Honore et al.
Structure-activity relationships in the development of excitatory amino acid receptor agonists and competitive antagonists.
Watkins et al.
Citations for DNQX disodium salt
The citations listed below are publications that use Tocris products. Selected citations for DNQX disodium salt include:
8 Citations: Showing 1 - 8
TMEM16B regulates anxiety-related behavior and GABAergic neuronal signaling in the central lateral amygdala.
Authors: Li Et al.
Single-cell transcriptomic analysis of mouse neocortical development.
Authors: Loo Et al.
Nat Commun 2019;10:134
Ethanol-Sensitive Pacemaker Neurons in the Mouse External Globus Pallidus.
Authors: Abrahao Et al.
Postnatal development of the electrophysiological properties of somatostatin interneurons in the anterior cingulate cortex of mice.
Authors: Pan Et al.
J Neurosci 2016;6:28137
Absence of plateau potentials in dLGN cells leads to a breakdown in retinogeniculate refinement.
Authors: Dilger Et al.
J Neurosci 2015;35:3652
Giant ankyrin-G stabilizes somatodendritic GABAergic synapses through opposing endocytosis of GABAA receptors.
Authors: Tseng Et al.
Sci Rep 2015;112:1214
Retinal input to efferent target amacrine cells in the avian retina.
Authors: Lindstrom Et al.
Proc Natl Acad Sci U S A 2010;27:103
Transient change in GABA(A) receptor subunit mRNA expression in Lurcher cerebellar nuclei during Purkinje cell degeneration.
Authors: Linnemann Et al.
Vis Neurosci 2006;7:59
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DNQX (20 micromolar) blocked spontaneous excitatory postsynaptic currents in an ex-vivo slice preparation.
We delivered this drug intracranially in combination with AP5 to block glutamatergic transmission in the mouse VTA. Product was highly soluble and worked well and as described, producing a robust decrease in place preference behavior.